FIGURE 8.

Schematic diagram illustrating the origin, phenotype and function of CXCR4⁺CD56^bright dNKs in maternal–foetal immune tolerance during early pregnancy. Trophoblasts attract peripheral CXCR4⁺ NK through secreting CXCL12. Trophoblasts further upregulate CD56 and downregulate CXCR4 expression of CXCR4⁺ pNK to adopt a dNK‐similar phenotype. CXCR4⁺CD56^bright dNK are the main source of IL‐4 at maternal–foetal interface, which induce CD4⁺CD45RA⁺ naïve T cells to preferentially differentiate to Th2‐type cells, involving in the maintenance of normal pregnancy. In miscarriage, the number and IL‐4‐prodution of CXCR4⁺CD56^bright NK cells in the decidua are compromised, which fail to promote Th2 bias at maternal–foetal interface